Cell Signaling Technology

Product Pathways - Angiogenesis

VWF (D8L8G) XP® Rabbit mAb #65707

No. Size Price
65707S 100 µl ( 10 western blots ) ¥3,580.00 现货查询 购买询价
65707 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human, Endogenous 310, 460 Rabbit IgG
IP 1:50
IHC-P 1:500

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, IP=Immunoprecipitation, IHC-P=Immunohistochemistry (Paraffin),

Specificity / Sensitivity

VWF (D8L8G) XP® Rabbit mAb recognizes endogenous levels of total VWF protein. This antibody recognizes both the VWF precursor and mature VWF.

Source / Purification

Monoclonal antibody is produced by immunizing animals with recombinant human VWF protein.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human prostate carcinoma using VWF (D8L8G) XP® Rabbit mAb.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using VWF (D8L8G) XP® Rabbit mAb (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower).

IP

IP

Immunoprecipitation of VWF from HUVEC cell extracts. Lane 1 is 10% input, lane 2 is Rabbit (DA1E) mAb IgG XP® Isotype Control #3900, and lane 3 is VWF (D8L8G) XP® Rabbit mAb.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human breast carcinoma using VWF (D8L8G) XP® Rabbit mAb.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human colon carcinoma using VWF (D8L8G) XP® Rabbit mAb.

Background

VWF (Von Willebrand factor) is a multimeric plasma glycoprotein that promotes adhesion of platelets to sites of vascular injury (1). Mature circulating VWF is made up of disulfide-bonded multimers that are in a complex with factor VIII (2). VWF is stored in secretory Weibel-Palade bodies in endothelial cells (3,4). It is synthesized as a large precursor protein and undergoes extensive posttranslational modifications including dimerization in the endoplasmic reticulum followed by cleavage of the pro-peptide and multimerization in the Golgi apparatus (3,4). VWF is important in hemostasis, and genetic defects in the structure and modification of VWF can cause von Willebrand disease (VWD), the most common congenital bleeding disorder in humans (5).  Alternatively, increased levels of VWF have been shown to be involved in acute coronary thrombosis and are a clinical risk marker for atherosclerosis (6). VWF has also been shown to have a role in inflammation, functioning as an adhesive site for a variety of leukocyte subsets (7). Through siRNA experiments and the use VWF-deficient mice, it has also been shown that VWF regulates angiogenesis (8).

  1. Tschopp, T.B. et al. (1974) J Lab Clin Med 83, 296-300.
  2. Hoyer, L.W. and Shainoff, J.R. (1980) Blood 55, 1056-9.
  3. Jaffe, E.A. et al. (1974) Proc Natl Acad Sci U S A 71, 1906-9.
  4. Wagner, D.D. et al. (1986) J Cell Biol 102, 1320-4.
  5. Sadler, J.E. (2005) Annu Rev Med 56, 173-91.
  6. Lip, G.Y. and Blann, A. (1997) Cardiovasc Res 34, 255-65.
  7. Pendu, R. et al. (2006) Blood 108, 3746-52.
  8. Starke, R.D. et al. (2011) Blood 117, 1071-80.

Application References

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Protocols

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For Research Use Only. Not For Use In Diagnostic Procedures.

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